Open Access Research article

Impairment of circulating endothelial progenitors in Down syndrome

Valerio Costa1, Linda Sommese2, Amelia Casamassimi3, Roberta Colicchio4, Claudia Angelini5, Valentina Marchesano6, Lara Milone7, Bartolomeo Farzati3, Alfonso Giovane7, Carmela Fiorito8, Monica Rienzo3, Marco Picardi9, Bice Avallone6, Massimiliano Marco Corsi10, Berardo Sarubbi11, Raffaele Calabrò11, Paola Salvatore12, Alfredo Ciccodicola1* and Claudio Napoli3

Author Affiliations

1 Institute of Genetics and Biophysics ''A. Buzzati-Traverso'', IGB-CNR, Naples, Italy

2 Section of Microbiology, Department of Experimental Medicine, 1st School of Medicine, Second University of Naples, Naples, Italy

3 Department of General Pathology and Excellence Research Center on Cardiovascular Diseases, 1st School of Medicine, Second University of Naples, Naples, Italy

4 IRCCS Fondazione SDN, Naples, Italy

5 Istituto per le Applicazioni del Calcolo, "Mauro Picone", CNR, Naples, Italy

6 Department of Biological Science, University of Naples "Federico II", Naples, Italy

7 Department of Biochemistry and Biophysics, Second University of Naples, Naples, Italy

8 IRCCS Multimedica, Milan, Italy

9 Department of Biochemistry and Medical Biotechnology, University of Naples "Federico II", Naples, Italy

10 Institute of General Pathology, Section of Clinical Pathology, Faculty of Medicine, University of Milan, Milan, Italy

11 Cardiology Department of Second University of Naples, "Monaldi Hospital", Naples, Italy

12 Department of Cellular and Molecular Biology and Pathology "L. Califano" and School of Biotechnological Sciences, University of Naples "Federico II", Naples, Italy

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BMC Medical Genomics 2010, 3:40  doi:10.1186/1755-8794-3-40

Published: 13 September 2010

Additional files

Additional file 1:

Supplementary Methods

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Additional file 2:

Table S1: Primer pairs used for quantitative and semi-quantitative RT-PCR

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Additional file 3:

Figure S1: Impaired EPC number and function. A) Representative photomicrographs of merged double-positive Dil-Ac-LDL/Lectin cells isolated from euploid (left panel) and DS (right panel) subjects (100X magnification). B) Fluorescence micrographs of EPCs labeled for 30 min with C11-BO in euploid and DS subjects. C) EPC number expressed as percentage in the different phases of cell cycle obtained by FACS. D) Curves indicate the percentage of EPC number infected with B. henselae in euploid and DS individuals. Results are representative of five different experiments in duplicate.

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Additional file 4:

Table S2: Chromosome 21 genes differentially expressed in DS vs euploids

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Figure S2: Distribution of differentially expressed genes along the human chromosomes (DS vs euploids). A) Bar graph showing the empirical frequency distribution of differentially expressed genes along the autosomes of DS progenitors vs euploids. Asterisks indicate the significantly deregulated chromosomes. B) Representation of the robustness of our findings shown in A. The left column shows the different user-defined fold-change. For each á value used in the analysis are shown the relative p-values. C) Bar graph showing the percent of differentially expressed genes along the DS autosomes.

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Additional file 6:

Figure S3: Positional gene mapping of differentially expressed genes (DS vs euploids). Graphic representation of positional gene enrichment (PGE) approach used to map differentially expressed genes in DS vs euploids EPCs to the exact location on the chromosome.

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Additional file 7:

Figure S4: B. henseale-induced gene expression in DS EPCs. A) Bar graph showing the top-scored deregulated gene pathways after infection in DS progenitors. Ratio indicates the percent of differentially expressed genes within the related pathway. B) Semiquantitative RT-PCR of Jak/STAT genes deregulated after B. henseale infection.

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Additional file 8:

Table S3: Differentially expressed genes after B. henselae infection

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